Giuseppe Cirino

TL;DR: The guidelines have been simplified for ease of understanding by authors, to make it more straightforward for peer reviewers to check compliance and to facilitate the curation of the journal's efforts to improve standards.

TL;DR: Inhibition of signalling through Hsp90 attenuates both agonist-stimulated production of nitric oxide and endothelium-dependent relaxation of isolated blood vessels and indicates that in addition to its role as a molecular chaperone involved in protein folding and maturation, HSp90 may also be recruited to cellular targets depending on the activation state of the cell.

TL;DR: Results suggest that endogenous H2S is an important mediator of acute inflammation, acting at the leukocyte‐endothelium interface, and have important implications for anti‐inflammatory drug development.

TL;DR: The goal of this review was to highlight the early research that led to the current understanding of the pathophysiologic role of NO in cardiovascular medicine and to discuss the possible mechanism of some drugs interfering with NO signaling cascade.

TL;DR: A chimeric peptide with a cellular internalization sequence fused to the caveolin-1 scaffolding domain was generated and systemic administration of the peptide suppressed acute inflammation and vascular leak to the same extent as a glucocorticoid or an endothelial nitric oxide synthase (eNOS) inhibitor.